Sasaki T, Kassell N F, Torner J C, Maixner W, Turner D M
Stroke. 1985 May-Jun;16(3):482-9. doi: 10.1161/01.str.16.3.482.
Pharmacological differences between canine and monkey basilar arteries were studied in vitro. The constrictor response of canine basilar artery to either norepinephrine or an alpha 1-adrenoceptor agonist phenylephrine was partly inhibited by an alpha 2-adrenoceptor antagonist yohimbine but not by an alpha 1-adrenoceptor antagonist prazosin. The contraction elicited by an alpha 2-adrenoceptor agonist clonidine was inhibited by neither prazosin nor yohimbine. These results suggest that the receptors in canine basilar artery which mediate norepinephrine-induced contraction are different from classical alpha 1 or alpha 2-adrenoceptors, although they more closely resemble the alpha 2- rather than the alpha 1-subtype. Using monkey basilar artery, phenylephrine produced the same amplitude of maximum contractile response as norepinephrine, though a much higher concentration of phenylephrine than norepinephrine was needed in order to elicit that maximum response. Clonidine did not elicit contractions. The contraction induced by norepinephrine was markedly suppressed by both prazosin and yohimbine in a noncompetitive fashion. The constrictor response of monkey basilar artery to norepinephrine, therefore, appears to be mediated by alpha 1-like adrenoceptors. Comparison of ED50 values for thromboxane A2 revealed that the monkey basilar artery was more sensitive to thromboxane A2 than that of the canine. Prostaglandin F2 alpha produced a larger maximum contraction in monkey basilar arteries than in canine basilar arteries, although the ED50 values for monkey basilar arteries were larger than those for canine basilar arteries. The ED50 values for serotonin in canine basilar arteries were a little less than those for monkey basilar arteries, although both arteries produced nearly identical maximum contractions.
对犬和猴的基底动脉的药理学差异进行了体外研究。犬基底动脉对去甲肾上腺素或α1肾上腺素能受体激动剂苯肾上腺素的收缩反应部分被α2肾上腺素能受体拮抗剂育亨宾抑制，但不被α1肾上腺素能受体拮抗剂哌唑嗪抑制。α2肾上腺素能受体激动剂可乐定引起的收缩既不被哌唑嗪也不被育亨宾抑制。这些结果表明，介导犬基底动脉去甲肾上腺素诱导收缩的受体不同于经典的α1或α2肾上腺素能受体，尽管它们更类似于α2亚型而非α1亚型。在猴基底动脉中，苯肾上腺素产生的最大收缩反应幅度与去甲肾上腺素相同，尽管为了引发该最大反应需要比去甲肾上腺素更高浓度的苯肾上腺素。可乐定未引起收缩。去甲肾上腺素诱导的收缩被哌唑嗪和育亨宾以非竞争性方式显著抑制。因此，猴基底动脉对去甲肾上腺素的收缩反应似乎由α1样肾上腺素能受体介导。血栓素A2的半数有效剂量（ED50）值的比较显示，猴基底动脉对血栓素A2比犬基底动脉更敏感。前列腺素F2α在猴基底动脉中产生的最大收缩比在犬基底动脉中更大，尽管猴基底动脉的ED50值大于犬基底动脉的ED50值。犬基底动脉中5-羟色胺的ED50值略低于猴基底动脉的ED50值，尽管两条动脉产生的最大收缩几乎相同。
